Oxidative stress and pyrogenic fever pathogenesis

doi:10.1016/j.ejphar.2011.05.075

Chia Nan University of Pharmacy & Science Institutional Repository > 環境永續暨休閒學院 > 休閒保健管理系(所) > 期刊論文 > Item 310902800/26717

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標題:	Oxidative stress and pyrogenic fever pathogenesis
作者:	Hou, Ching-Cheng Lin, Hung Chang, Ching-Ping Huang, Wu-Tein Lin, Mao-Tsun
貢獻者:	休閒保健管理系
關鍵字:	Pyrogen Fever Glutamate Nitric oxide metabolite Hydroxyl radical
日期:	2011-09
上傳時間:	2013-06-21 16:52:29 (UTC+8)
出版者:	Elsevier
摘要:	The causative/regulatory connections between changes in tissue redox state and fever induction were investigated herein. Wherefore, LPS, the primary element of bacterial cell wall, in addition to inducing pro-inflammatory cytokines, activated macrophages and other leukocytes to secrete hydroxyl radical (OH), nitric oxide metabolites (NOx−), superoxide (O2) and other reactive oxygen/nitrogen species. Furthermore, inflammation response-associated hypoxia stimulated glutamate release, which caused excitotoxicity of cells by increasing extracellular Ca2+. Cytokines and glutamate in turn also triggered the release of large amounts of NOx−, OH, O2, and other radicals. Those reactive nitrogen species in turn caused cellular injury via the peroxidation of membrane lipids and oxidative damage of proteins and DNA. Glutamate, NOx−, OH and antioxidants participated in the pathogenesis and regulation of LPS- or cytokines-induced fever. In particular, to highlight the role of glutamate, prostaglandin E2, NOx− and OH generated in the hypothalamus during pyrogenic fever was attempted hereby. To find the link among the signaling with the glutamate, NOx− and OH/prostaglandin E2 in the hypothalamus during pyrogenic fever will be challenging and could now clinically suppress pyrogenic fever.
關聯:	European Journal of Pharmacology 667(1-3), pp. 6-12
显示于类别:	[休閒保健管理系(所)] 期刊論文

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